This Nutrient Improves Night Driving

Eyes function differently based on the level of light in the environment. In normal daylight the eye primarily uses cones to focus the light. In near darkness, the eye primarily uses rods to focus the light. Low light conditions such as driving at night require both mechanisms. Lutein is an orange-red carotenoid pigment produced by plants and is present in the diet in colorful fruits and vegetables. One of the best sources of lutein is kale which provides more than 20 mg per cup. Cooked spinach, collard greens and turnip greens also pack a similar punch. This compares to romaine lettuce and raw spinach which have less than 4 mg of lutein available for use.

In the body, lutein is one of the predominant pigments concentrated in the macula, a specialized area of the eye that is responsible for central vision. In addition, it is known to be deposited in the skin. It is thought that lutein’s functional role in these vulnerable tissues is to protect against sunlight-induced free radical production.

Ever since the Blue Mountain Eye Study reported that higher dietary lutein and zeaxanthin intake reduced the risk for incident of age-related macular degeneration (AMD) over 5 and 10 years, significant interest has been placed on these particular carotenoids.[1]

In an interesting study, middle-aged adults who drove for a living (i.e. taxi drivers) were given 20 mg of lutein or a placebo for one year. Researchers measured a variety of outcomes including something called macular pigment optical density (MPOD) [2] MPOD has been associated with improvements in visual function in those with age-related macular degeneration.[3]

This study showed that supplemental lutein, at this dose, increases serum levels of lutein.  However, of key importance is the length of the study and the measurement of vision performance. Under low light conditions, the group receiving treatment of lutein performed better at testing of contrast sensitivity and glare sensitivity. MPOD was also increased.

No significant side effects were reported in this study. Carotenodermia is one concern of large doses of carotenoids and while transient and relatively harmless, it was not seen in this study.  Previous studies have considered doses of 6 and 12 mg and showed peak serum lutein levels after 3-6 months^{.[4], [5], [6], [7]} However, in this research, peak levels were seen after just 30 days. This was attributed to the higher dose and good compliance among participants. While following serum levels of a specific carotenoid often does not typically have clinical value, uptake of lutein by the macula can take several months following peak levels. Indeed, this effect was seen in this study as well. Despite seeing a six-fold increase in serum levels after only one month, visual performance did not improve until three months after initiation of lutein administration. While 6 mg did not improve macular pigment optical density (MPOD) in previous studies, this study confirmed increases in this valuable biomarker.⁴ Several hypotheses remain about how macular pigment plays a role in the health of the eye but a leading theory is that antioxidants in the pigment reduce oxidized products produced by the interaction of light and tissues.

One of the challenges of the study was that serum levels of lutein in the participants at baseline were found to be lower than expected. It is thought that profession or economic status could play a role in this. Unfortunately, it creates another question. If a person already has adequate lutein levels in serum, will they not benefit from supplementation? This remains to be determined.

Another question that may arise concerns other carotenoids. The family of carotenoids (including beta carotene, alpha carotene, astaxanthin, zeaxanthin and others) may compete for absorption and excess dosing of a single carotenoid may hypothetically lead to insufficiencies among the other phytonutrients. Unfortunately, serum levels of these other carotenoids were not measured at baseline or throughout the study.

Essentially, participants taking lutein in this study could not read a Snellen chart, the tool with the large E at the top that optometrists and physicians use, any better than the placebo group after a year of use. Visual acuity was not significantly different. However, seeing movement in the periphery under low light conditions was improved. This is interesting because visual performance is more of a real-life analysis. Especially in this demographic studied, those whose job requires long hours of driving, even minor improvements in vision can result in improved driving performance and safer roads. Up to 23% of car accidents have been associated with reduced visual performance.[8] The challenge of the results of this study is the age-group that was studied. Young to midlife adults are not often the ones commonly complaining of decreased night vision. More often than not, the aging person no longer trusts their ability to navigate in low light conditions and this may result in decreased activity and a lower perceived quality of life. As people age, reduced participation in activity is a concern for incidence of depression. Those who continue to drive despite declining vision are putting themselves and others at risk. It would be curious to see if similar results could be replicated in an older population. Until that result is published, people may find this relatively inexpensive and safe intervention worth a one year trial for themselves.

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[1] Tan JS,Wang JJ, Flood V, Rochtchina E, SmithW, Mitchell P. Dietary antioxidants and the long-term incidence of age-related macular degeneration: the Blue Mountains Eye Study. Ophthalmology 2008;115(2):334–41.

[2] Lutein supplementation improves visual performance in Chinese drivers: 1-year randomized, double-blind, placebo-controlled study. Nutrition (2013), http://dx.doi.org/10.1016/j.nut.2012.10.017

[3] Weigert G, Kaya S, Pemp B, Sacu S, Lasta M, Werkmeister RM, Dragostinoff N, Simader C, Garhöfer G, Schmidt-Erfurth U, Schmetterer L.Effects of lutein supplementation on macular pigment optical density and visual acuity in patients with age-related macular degeneration. Invest Ophthalmol Vis Sci. 2011 Oct 17;52(11):8174-8. doi: 10.1167/iovs.11-7522.

[4] Sasamoto Y, Gomi F, Sawa M, Tsujikawa M, Nishida K. Effect of 1-year lutein supplementation on macular pigment optical density and visual function. Graefes Arch Clin Exp Ophthalmol 2011;249:1847–54.

[5] Ma L, Lin XM, Zou ZY, Xu XR, Li Y, Xu RA. 12-week lutein supplementation improves visual function in Chinese people with long-term computer display light exposure. Br J Nutr 2009;102:186–90.

[6] Nolan JM, Loughman J, Akkali MC, Stack J, Scanlon G, Davison P, et al. The impact of macular pigment augmentation on visual performance in normal subjects: COMPASS. Vision Res 2011;51:459–69.

[7] Olmedilla B, Granado F, Blanco I, Vaquero M. Lutein, but not alpha-tocopherol, supplementation improves visual function in patients with age-related cataracts: a 2-y double-blind, placebo- controlled pilot study. Nutrition 2003;19:21–4.

[8] Ranny T. Psychological factors that influence car-following and car following model development. Transportation Res 1999;Part F 2:213–9.

Melatonin and Type II Diabetes

In a study observing 370 women (nurses) who developed diabetes between 2000 and 2012 and 370 women (also nurses) who did not develop diabetes during this time frame the major urinary metabolite of melatonin (6-sulfatoxymelatonin) was measured against urinary creatinine. This was a part of the Nurses' Health Study cohort.[1]

This study provides a correlation between the lowest level of melatonin metabolite secretion and the development of type 2 diabetes. Women with the highest excretion of 6-sulfatoxymelatonin developed diabetes at a rate of 4.27 cases per 1000 while women with the lowest excretion of 6-sulfatoxymelatonin developed diabetes at a rate of 9.27 cases per 1000. This provides 2.17 times the risk for development of type 2 diabetes for those with low excretion.

Upon the initial publication of these results, two immediate camps developed. One camp, excited to explore the therapeutic uses of supplemental melatonin and then another that dismissed the data due to the nature of the study. It is correct to indicate that this information alone does not allow for mass medication of those with type 2 diabetes or for use in prophylaxis. However, researchers did an excellent job of addressing confounding issues within the scope of known physiologic mechanisms.

With diabetes on the rise, and 1 in 10 American adults wielding the diagnosis, this information is welcomed if it is interpreted correctly and cautiously.

The first question that must be addressed is if urinary excretion of 6-sulfatoxymelatonin is an adequate surrogate for nocturnal melatonin secretion from the pineal gland. Secretion of melatonin follows a daily pattern peaking 3-5 hours after sleep onset when it is dark with almost no production during daylight. Fortunately, the urinary excretion of 6-sulfatoxymelatonin when normalized to urinary creatinine has been used to estimate overnight melatonin secretion. This is good news since nocturnal plasma evaluation is impractical in the outpatient setting.[2]^,[3] Of interest is that this same biomarker was used to provide evidence for a statistically significant inverse association between melatonin levels, as measured in overnight morning urine, and invasive breast cancer risk in postmenopausal women.[4]

The next question may be in regards to the relationship between disrupted sleep and type 2 diabetes.[5] Researchers noted sleep disruption by two factors: snoring and sleep duration. Both of these factors were self-reported which may lead to limitation of information.

Another question arises in regards to the mechanism of how melatonin, a hormone typically associated with sleep directly affect glucose metabolism. Researchers suggest it may have to do with insulin secretion but human studies are lacking in this area. Most research is done on rodents and this is potentially problematic. Rodents are primarily nocturnal creatures and have different circadian patterns. While rats and mice may derive specific health benefits from exogenous administration of melatonin, it doesn’t always mean that humans will derive the same benefit to the same magnitude. However, the work that has been done so far piques curiosity. Oral consumption of melatonin protected rats prone to diabetes from developing increased cardiovascular and diabetes risk markers while being fed a high-calorie diet.[6] Melatonin administration to insulin-resistant mice reversed insulin resistance and improved glucose metabolism.[7] Human in-vitro studies have pointed to a kinase pathway that supports pancreatic islet cells.[8]^,[9],[10]

While some may discount summarily the study because it is done with nurses, all women, mostly (97%) Caucasian, and prone to shift work, that may be a premature dismissal. Interestingly, the nurses involved in this nested group of the Nurses’ Health Study reflected very little shift work perhaps due to age and seniority. It is true though that results can only be attributed to women and a limited racial heritage.

So while it is too early to suggest the use of melatonin as adjunctive care to glucose metabolism, it will likely be several years before type, dose, and timing of administration will be available in the peer-reviewed literature. One thought in integrative medicine is to normalize levels similar as how vitamin D is often recommended rather than a set dose. However, no agreed upon reference range has been established for urinary 6-sulfatoxymelatonin: creatinine although the highest quartile in this study had a median ratio of 67.0 ng/mg. Because melatonin is a hormone from outside of the body, the recommendation of lowest effective dose may apply similarly to the recommendation of hormone therapy.[11]

While melatonin may not be ready for the lime-light in diabetes, low-dose melatonin is something to keep in mind when caring for those patients at risk or suffering from the condition.

Natural Health International is the proud manufacturer and distributor of Herbatonin the first plant-based melatonin available in 3 mg and 0.3 mg

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[1] McMullan CJ, Schernhammer ES, Rimm EB, Hu FB, Forman JP. Melatonin secretion and the incidence of type 2 diabetes. JAMA. 2013 Apr 3;309(13):1388-96. doi: 10.1001/jama.2013.2710.

[2] Lang U, Kornemark M, Aubert ML, Paunier L, Sizonenko PC. Radioimmunological determination of

urinary melatonin in humans: correlation with plasma levels and typical 24-hour rhythmicity. J Clin Endocrinol Metab. 1981;53(3):645-650.

[3] Baskett JJ, Cockrem JF, Antunovich TA. Sulphatoxymelatonin excretion in older people: relationship

to plasma melatonin and renal function. J Pineal Res. 1998;24(1):58-61.

[4] Schernhammer ES, Berrino F, Krogh V, Secreto G, Micheli A, Venturelli E, Sieri S, Sempos CT, Cavalleri A, Schünemann HJ, Strano S, Muti P. Urinary 6-sulfatoxymelatonin levels and risk of breast cancer in postmenopausal women.J Natl Cancer Inst. 2008 Jun 18;100(12):898-905. doi: 10.1093/jnci/djn171. Epub 2008 Jun 10.

[5] Wagner, Kelly. "Sleep Laboratory Finds Insomnia With Short Sleep Duration Is A Risk Factor For Diabetes." Medical News Today. MediLexicon, Intl., 11 Jun. 2009. Web.

13 May. 2013. <http://www.medicalnewstoday.com/releases/153361.php>

[6] Prunet-Marcassus B, Desbazeille M, Bros A, et al. Melatonin reduces body weight gain in Sprague Dawley rats with diet-induced obesity. Endocrinology. 2003; 144(12):5347-5352.

[7] Cuesta S, Kireev R, Garcı´a C, Rancan L, Vara E, Tresguerres JA. Melatonin can improve insulin resistance and aging-induced pancreas alterations in senescence-

accelerated prone male mice (SAMP8). Age (Dordr). 2012.

[8] Kemp DM, Ubeda M, Habener JF. Identification and functional characterization of melatonin Mel 1a

receptors in pancreatic beta cells: potential role in incretin-mediated cell function by sensitization of cAMP signaling. Mol Cell Endocrinol. 2002;191(2):157-166.

[9] Ramracheya RD, Muller DS, Squires PE, et al. Function and expression of melatonin receptors on human pancreatic islets. J Pineal Res. 2008;44(3): 273-279.

[10] Picinato MC, Hirata AE, Cipolla-Neto J, et al. Activation of insulin and IGF-1 signaling pathways

by melatonin through MT1 receptor in isolated rat pancreatic islets. J Pineal Res. 2008;44(1):88-94.

[11] http://www.fda.gov/forconsumers/byaudience/forwomen/ucm118624.htm

Caffeine Withdrawal Now a Mental Disorder

While many of us thought that paying $5 for a tasty herbal beverage was the real mental disorder, we’ll have to wait for the next psychiatric manual for that diagnosis because a new one is on the table.

If you are a committed coffee drinker or enjoy a few too many caffeinated sodas or drinks on the weekends and are considering modifying your habits, your morning routine and entire world as you know it now has new implications. You may be crazy.

The DSM-V (American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders version five) has a quirky new diagnosis that may affect you. It is called withdrawal from caffeine intoxication. The diagnosis is well meaning. People who consume 250 mg of caffeine can experience caffeine intoxication and can fundamentally change their brain chemistry and the withdrawal period of this drug, yes drug, is now a listed and recognized diagnostic mental disorder. How much is 250 mg?

·      12 ounces (Tall) Starbucks Coffee            

·      32-56 ounces of green tea, brewed for 3 minutes            

·      100 ounces of most sodas (5 – 20 ounce bottles)

·      1.5-16 ounce cans of most energy drinks

·      1.9 ounces of 5-Hour Energy (contains about 208 mg)

Caffeine-related disorders include intoxication which first made it into the DSM-IV in 2011 with symptoms of restlessness, nervousness, excitement, insomnia, flushed face, excessive urination (diuresis), gastrointestinal disturbance, muscle twitching, rambling flow of thought and speech, tachycardia or cardiac arrhythmia, periods of inexhaustibility or unintentional motion (psychomotor agitation).

Caffeine withdrawal and its inclusion as a mental disorder started rumbling almost 10 years ago when an article appeared in Psychopharmacology where researchers from American University (Washington, DC a bastion of caffeine consumption) wrote about the symptoms of withdrawal including

·       Headache

·       Fatigue

·       Decreased energy/activeness

·       Decreased alertness

·       Drowsiness

·       Decreased contentedness

·       Depressed mood

·       Difficulty concentrating

·       Irritability

·       Foggy/not clearheaded

·       Flu-like symptoms

·       Nausea/vomiting

·       Muscle pain/stiffness

With a list of symptoms like this, I’m starting to believe this should be included in the manual. They go on to say “the incidence of headache was 50% and the incidence of clinically significant distress or functional impairment was 13%.” Those are high numbers for withdrawal from a widely available, freely distributed, and highly utilized drug.  

During the first few days of withdrawal, those who drop caffeine cold turkey display all of the tell-tale signs of an addict. They often search for every version of “coffee-methadone” they can find. Yes, the symptoms are transient, but they are intense. Headache and irritability top the symptom list.

What is interesting to me is that they noted that these symptoms of caffeine withdrawal tend to occur 12-24 hours after the high and continue for 2-9 days.

And this may come as no shock, but the higher the daily dose of caffeine, the worse the symptoms. What I found really curious is that symptoms were caused by doses as low as 100 mg. They concluded, mind you, this is 2004, “The caffeine-withdrawal syndrome has been well characterized and there is sufficient empirical evidence to warrant inclusion of caffeine withdrawal as a disorder in the DSM and revision of diagnostic criteria in the ICD.” It is 2013 and now it is included. So instead of being shocked, maybe we should be appalled at how long this inclusion took!

There is a take home point. For those who are embarking upon a new detoxification program, a new health habit, or simply shifting your gears in relation to the food, supplements, or medications you are using, please remember that it is not always the addition of a substance that causes symptoms, but it can also be the removal of substances that causes symptoms (or improvements). So, don’t just tell your healthcare practitioner what you started to fix your problem, but also tell them what you stopped. 

Reference: Juliano LM, Griffiths RR. A critical review of caffeine withdrawal: empirical validation of symptoms and signs, incidence, severity, and associated features. Psychopharmacology (Berl). 2004 Oct;176(1):1-29. Epub 2004 Sep 21.

Thinking Twice About Testosterone Replacement

Testosterone replacement therapy can be a necessary medical intervention in some men for conditions such as sexual dysfunction, depression, and chronic fatigue. However, there are known risks. Popularity of testosterone prescriptions are skyrocketing, but who is it safest for and who is at the greatest risk of early cardiovascular death and heart attack? How do consumers make decisions in combination with their doctor without knowing the consequences? Ultimately you have to rely on the experience and knowledge of your provider, but having the right information in front of you can only help the decision process.

In a recent publication from Endocrine Today, evidence suggests that a new subset of men should not use testosterone replacement therapy. Men with obstructive coronary artery disease have higher risk of death and heart attack when using testosterone replacement therapy.

But that leaves some questions, doesn't it? What if you've had a coronary angiograph which confirmed obstruction or perhaps had an angioplasty or stent to correct obstruction and also have confirmed or suspected low testosterone levels? Are you just out of luck with no therapy for the hormone imbalance?

Symptoms of hormone imbalance in aging men are not limited to sexual dysfunction. Rather, depression, poor sleep, poor recovery from activity, poor stamina, libido (sex drive), lack of energy, and decreased strength and performance may all be symptoms of hormone imbalance. We also note that stress and poor blood sugar control can deteriorate men's hormones at an accelerated rate as well. Does this sound familiar? If so, read on.

We often suggest lifestyle modification such as weight loss, stopping smoking, and increasing exercise, especially activities such as weight training and sprinting to improve hormone balance in aging men, but the reality is that besides stopping smoking, these are quite tall orders for those who have obstructive coronary artery disease. Thirty minutes of weight lifting or daily sprinting probably isn't going to be approved by the cardiologist or cardiac rehab therapist. Not to mention that poor hormone balance often makes losing weight difficult.

Getting back to the basics of health, the pillars of good living, may be the answer along with specific products to support hormone balance.

From a diet perspective, adequate protein is an absolute must to stop the breakdown of muscle in aging men. Supplemental protein shakes are often a good way to go if appetite isn't great or cooking isn't your strong suit. If you can tolerate whey protein, it seems to be one of the best sources. It raises glutathione levels which is important from an antioxidant perspective and also contains branch chain amino acids which support muscle health. Vegan protein powders are a bit easier on the body. These contain hemp, pea, and/ or rice but often times are much lower in protein content. Shoot for 20 grams per shake. Nuts and seeds provide excellent protein from plant sources as well. Vegetable and plant nutrients cannot be understated for general heart health and all doctors and practitioners should be encouraging this behavior.

From a dietary supplement side, Revolution Macalibrium is a tested formula of specific phenotypes of maca (Lepidium peruvianum). Maca has a rich history of supporting men's hormone health; however, research has shown that there are specific phenotypes ideal for men’s hormonal health. Revolution Macalibrium not only has these exact phenotypes but has concentrated levels of the full spectrum of active constituents ten to twenty times higher than the levels found in raw maca which is why doctors and patients are getting such strong results quickly. This is a foundational product that works through the hypothalamus-pituitary-adrenal axis to help a man make his own hormones versus relying on hormones from outside of the body. A man's own hormones made by him is much safer since nothing is more natural than your own hormones.

Omega-3 fatty acids, especially those rich in EPA and DHA are recommended. If a man has high triglycerides, the American Heart Association suggest 2.4 grams of EPA + DHA per day. This seems like a prudent suggestion for all men facing either hormone imbalance, obstructive coronary artery disease, or life in the modern world. Reducing inflammation and supporting cell membrane health are just two well known mechanisms of omega-3 fatty acids and since the human body doesn't make its own omega-3's it has to rely on us to ingest them every day. I prefer high EPA products. Some products contains as much as 1060 mg of EPA and 274 mg of DHA per 2 capsules. Two capsules twice per day is ideal to hit this goal dose of 2.4 grams. Be wary of lower doses or you'll end up taking 8 capsules per day. Many products will contain 180 mg of EPA and 120 mg of DHA. This is perhaps suitable for the percentage of the population that gets nearly adequate dietary omega-3 fatty acids and is already healthy.

Other interventions and supplements may be indicated given your history and complicating factors, and in that case we recommend working with a doctor who understands your condition and also natural approaches. Click here to find a practitioner close to you.

So, if you know a man considering testosterone replacement and also has obstructive coronary artery disease, arm them with this important information so he can make an empowered decision.

On Your Feet, Thyroid?

If you have a thyroid condition, you probably wish you could  whip it into shape in a few weeks of hard work, like a Boot Camp. But drill sergeants and obstacles courses are not what your thyroid needs. Think of your thyroid gland as your friend who cries at movies and hems and haws over rather small life changes. It is, like your friend, sensitive to feedback. 

When the thyroid is screaming for trouble, don't forget about its compadres (other organs) that offer direction and guidance to the thyroid gland.

• Gall bladder function impacts the thyroid gland because poor gall bladder function keeps the all important fat soluble vitamins from working. (Lots of thyroid sufferers have had gall bladder surgery). The gall bladder secretes bile, a necessary substance to take in vitamins A, D, E, and K.  If your gallbladder is bile deficient or you have had it removed, you may not be absorbing enough fats resulting in a lack of fat soluble vitamins like Vitamins A, D, E, and K. Your thyroid and adrenals needs vitamin A to work correctly and efficiently. Not just beta carotene but good old-fashioned, preformed vitamin A! Check your multivitamin as to the source of its Vitamin A. Post-surgically, I recommend micellized forms of vitamin A, D, E, and K.

• Digestive function modulates thyroid function as well as it is intimately involved with the immune system (lots of gluten sensitivity in thyroid sufferers). If you have any type of digestive dysfunction from heartburn to gas, diarrhea or constipation, addressing the root cause of it is important. Oftentimes, a pH balanced diet, probiotics, and stress reduction are the first steps to fixing a busted digestive system.

• Hormone balance is also key in both men and women with thyroid dysfunction. Low progesterone can actually hide the fact that a sluggish thyroid is actually a more sinister form called Hashimoto's Thyroiditis. As estrogen declines so too does thyroid function. So much so that a reported 30% of postmenopausal women suffer from hypothyroidism.

• Belly fat. That's right, fat is an organ too. Extra weight around the middle negatively impacts thyroid function. The more fat you have on your frame, the more inflammatory signals you release to the rest of your body. 

So where do you start? Well, you can't send your friend to Boot Camp and yell at them to be tough....you have to strengthen them. Revolution Macalibrium for men and Femmenessence for women are ideal foundational products to strengthen the stress response system in addition to meditation, proper sleep, and a diet rich in plant nutrients. Femmenessence has specific formulations for perimenopausal women and reproductive-aged women as well. These products help your thyroid gland but supporting a myriad of hormones in the body. Every hormone imbalance including stress hormone imbalance directly impacts thyroid function.

Realize that this is a place to start with thyroid conditions. Reducing fat through a primarily plant-based diet, resistance training, and supporting all organs through stress reduction and proper supplementation are all pieces to a potentially complex puzzle. For more information about these products or concepts, contact corey.schuler@naturalhi.com

Updated evidence on menopause hormone therapy

A recent panel has re-evaluated the scientific literature since  the 2001 publication of the Women’s Health Initiative in order to determine if hormone replacement therapy is safe long term and for chronic conditions such as bone loss, cardiovascular risk, and / or mood health. The results of this panel are from critical review of 51 published articles and will guide the standard of care for postmenopausal women. Frankly, we’ve learned a lot in the last 11 years and I think this panel did an excellent job of culling the data albeit falling short of offering reasonable and safe solutions to the challenge of increased risk of chronic disease beginning at menopause. But that's okay. It wasn't their goal. 

http://health.usnews.com/health-news/news/articles/2012/05/28/hrt-update-therapy-may-reduce-fractures-boost-some-risks

In full disclosure, I’m an advocate of natural products so my first inclination is the cheer the panel’s recommendation. It has been my read of the last decade of literature as well. However, it is oversimplified to come to the conclusion that HRT is good or HRT is bad. That binary way of thinking is ruinous. I strongly believe there is a definite place for Hormone Replacement Therapy. I also believe it cannot be used as the panacea it once was thought to be. In the case of bone health, we must be ever mindful of the complete physiology. Sure, estrogen inhibits osteoclastic activity and helps to maintain bone mineral density, but other hormones have a role in osteoblastic activity such as progesterone and testosterone. Growth hormone and cortisol have their own effects partially independent of sex hormones and partially dependent on their levels.  Furthermore, we now have evidence that bone morphogenetic proteins, progenitor cells for bone, have cross talk with estrogen and there may be other unknown interactions to other hormones and signals. Some authorities now place osteopenia and osteoporosis, especially precocious bone loss in the inflammatory disease marker, causing us to work through the contribution of cytokines and prostaglandins whose pathways are influenced by estrogen levels. And this is just bone health, not to mention cardiovascular health and other quality of life issues that are also influenced by hormone status. Why is this important to say? Because, we haven’t heard the last of HRT. We will likely come to understand a further undeclared subpopulation that has little to no risk of cancer and cardiovascular incident. However, we aren’t there yet and we have patients in front of us that need our help. This panel’s recommendation brings us one step closer to the truth. What is missing from the conversation and really outside the scope of this article is the reason for hormone imbalance and potential less risky recommendations that clinicians can make today to support not only the symptoms of menopause but also the long term consequences of hormone loss. Personally, I’ve been involved in understanding this exact mode of action. That is, improving the function of what has become known as the HPA or hypothalamus-pituitary-adrenal axis. In fact, there are several axes that we should be aware of that are influenced by an aging hypothalamus. These axes, but particularly the HPA, when supported can stimulate the body’s own production and balance of hormones. In essence, improving this system allows the feedback and control of hormone production to be self-regulating without the burden to liver biotransformation that exogenous hormones appear to have. When a post-menopausal woman can improve her ability to produce her own hormones with changes in menopausal symptoms, bone mineral density scores, and cardiovascular support, then we have something to write about. This approach can be used in conjunction with hormone therapy in order to be in line with the recommendation of smallest dose, shortest duration of time. This is the question that should be asked. “What can we do, today, for women to be on the smallest dose of hormone replacement for the shortest amount of time and still retain quality of life?” The question should not be “is HRT good?”. More research into patient selection criteria is warranted. However, what I’m afraid will happen, at the expense of quality patient care, is disregard for these recommendation with some clinicians refusing to prescribe and others continuing to over-prescribe. We want something with a broad therapeutic window with no history of safety concerns. Something that supports endogenous hormone production so that lowest dose, shortest duration can be honored. We want something that has clinical trials that support efficacy in a broad spectrum of conditions the way HRT does. What we want exists and is available on the market as a natural product. Femmenessence (Maca-GO®) is that commercially available natural product. The following is a technical/ White Paper on the evidence of Femmenessence (Maca-GO®) http://naturalhi.com/downloads/WhitePaper_MacaGO.pdf and links to the abstracts of the peer-reviewed journal articles referenced http://naturalhi.com/Post-Menopause.aspx

They make you fat…and they aren’t food!

What do new car smell, your favorite fragrance, and a plastic bottle have in common? Well, while it sounds like a bad joke, it is quite serious. Each of these and many other common products contain substances called obesogens. That’s right, chemicals that initiate or propagate obesity. Of course, diet and exercise are still real contributors to weight, but the body composition equation runs a coefficient of hormone balance and obesogens disrupt hormone balance….sometimes in a big way!  And don’t think that just because you maintain healthy body weight that this doesn’t apply to you. Obesogens are endocrine disruptors and are the same chemicals that contribute to hormone issues such polycystic ovarian syndrome, amenorrhea, low testosterone, infertility, increased perimenopausal and menopausal symptoms, and certain cancers regardless of what the scale says.

Plasticizers leach from carpets and newly installed car interiors, thus providing that ever so pungent new car smell. In fact, when working with a hormone imbalance patient, I ask questions about exposure to new carpets and cars and after the weird looks, I get the story and excitement of a new “thing”, and then another weird look. Although, more often than not symptoms started or got worse after the new purchase.

If you’re thinking this is just another made up term to scare us or another excuse to rationalize dietary indiscretion, you would be misinformed. Obesogen is a term first coined in 2002 and since then has been cited in 19 peer-reviewed articles, with 6 of those published in 2011 and 4 already in 2012. It is gaining understanding and isn’t going away.

Much like we are learning that certain phytonutrients speak directly to our own genetic material, the hypothalamus, our master gland, and may either potentiate or interfere with enzymes, so too do these environmental chemicals.

The following are four truths as found in the Journal of Andrology:

• “Obesogens are chemicals that directly or indirectly lead to increased fat accumulation and obesity. 
• Obesogens have the potential to disrupt multiple metabolic signaling pathways in the developing organism that can result in permanent changes in adult physiology.
• Prenatal or perinatal exposure to obesogenic endocrine disrupting chemicals has been shown to predispose an organism to store more fat from the beginning of its life.
• This suggests that humans, who have been exposed to obesogenic chemicals during sensitive windows of development, might be pre-programmed to store increased amounts of fat, resulting in a lifelong struggle to maintain a healthy weight and exacerbating the deleterious effects of poor diet and inadequate exercise.”[1]

So it really may be true that some people are literally programmed to be fatter. However, that doesn’t mean that it is inevitable or uncontrollable. We are all dealt a different deck. Not all of us have the genetic material to be Olympic athletes and some that do, do not participate in the required training to compete, thus illustrating the contributions of both how we were made and what we’re exposed to. Where this becomes vitally important is during the reproductive years. Preconception programs often address helping moms-to-be and dads-to-be engage in healthy behaviors, optimizing hormone levels, improving detoxification, and reducing exposures to toxins. This is one such sensitive windows where obesogens can wreak havoc on metabolism…prior to conception!

The list of obesogens include phthalates also known as plasticizers are also found in personal care products such as shaving creams, colognes, and lotions, Bisphenol A (BPA) is found in plastic bottles and polyvinylchlorides found in shower curtains.

Recent changes at Whole Foods Market address possible concerns with obesogens. Dr. J. Renae Norton describes these changes in a two part series (Part I and Part II).

However, you can drive yourself crazy thinking about avoiding these chemicals. Most of them are released for absorption through your skin or ingested when plastics are heated. Avoiding hot plastics is a good step in the right direction but total avoidance is likely not possible with these nearly ubiquitous chemicals. Additionally, though, you can support the excretion of these chemicals through supporting liver, kidney, and bowel function on a daily basis.  Glutathione levels are perhaps most important if we zoom in single markers of the body. Glutathione acts as a free radical scavenger and also supports liver function. Without the bowel and kidneys functioning at their best, these chemicals cannot be eliminated. Supporting kidney function can be done with Sole therapy using Original Himalayan Crystal Salt and pH Quintessence on a daily basis. The pH Quintessence product also supports liver function, glutathione levels and bowel motility, making it a versatile and easy to use product. While obesogens may have programmed you to gain weight faster than normal and caused hormone imbalance, supporting the hypothalamus, the master gland, can help send the right signals to the right glands that need help the most while your body restores homeostasis. The hypothalamus talks to the pituitary gland and these two partners then communicate to the thyroid gland, pancreas, adrenal glands, ovaries, and testes. Natural Health International has introduced products for men well as different stages of life for women (Premenopausal, Perimenopausal, and Postmenopausal) to support comprehensive endocrine balance without introducing hormones from outside the body but rather supporting hypothalamus and pituitary function and all their downstream metabolic effects.

Obesogens are a serious chemical insult, but with some awareness of their effects, can be minimized and our bodies fully supported.

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[1] Janesick A, Blumberg B. Obesogens, stem cells and the developmental programming of obesity. Int J Androl. 2012 Feb 28. doi: 10.1111/j.1365-2605.2012.01247.x.